Transluminal Angioplasty — Pathologic Basis

Abstract

The mechanism of success in transluminal angioplasty — whether by dilatation (of narrow but patent lumen) or recanalization (creation of a neolumen in occluded artery) — resides in the physical properties of the obstructive lesion(s), and the outcome of treatment is influenced by the character as well as the distribution of lesions in each patient. In the ideal therapeutic situation, obstruction is the immediate result of a localized, primary, atheromatous transformation of the normal intima into a firm, mostly acellular, amorphous, collagenous core encroaching upon the lumen and surrounded by relatively normal elements of the arterial wall (Fig. 1). This core, though often widely present within larger arteries, tends to obstruct at characteristic sites, such as the aortic, iliac, and carotid bifurcations, the proximal coronary arteries, and the adductor hiatus segment of the superficial femoropopliteal artery, thus providing evidence that hemodynamic (as well as metabolic, cultural, dietary, inheritable and other) factors play etiologic roles. Whatever the role of hydraulic stress, it is a fortunate fact that frequently in early, uncomplicated stages of the disease, arteries distal to local obstructions tend to be less affected, possibly because of a protective effect of the proximal stenosis.